Chem Path: AKI and CKD

Question 1

How is creatinine used to stage AKI

Answer 1

Constant measurement of sCr to see how it changes. One off measurement is not useful, Stages 1 2 and 3

Question 2

What is the hallmark of pre renal AKI

Answer 2

Reduced renal perfusion

Question 3

Why can there be reduced renal perfusion

Answer 3

True volume depletion - dehydration, D&V, bleed
Hypotension
Oedematous stress such as HF
Renal ischaemia such as renal artery stenosis
Drugs

Question 4

What drugs affect renal perfusion and how so

Answer 4

NSAIDs and calcineurin inhibitors - Decrease afferent arteriole dilatation
ACEi and ARBs - Decrease efferent arteriole constriction
Diuretics - Decrease preload and affect tubular fx

Question 5

What is normal serum creatinine levels?

Answer 5

59 - 104 males

49 - 84 females

Question 6

How does pre renal AKI differ from Acute Tubular Necrosis (ATN)

Answer 6

Pre renal AKI will resolve once the cause is addressed and the circulation volume is restored. Prolonged injury causes hypoxic necrosis and can lead to ATN. ATN does not respond to recirculating volume.

Question 7

What can you see on ATN urine microscopy

Answer 7

Epithelial cell casts

Question 8

Why would you see hydronephrosis on kidney USS

Answer 8

Benign prostatic hypertrophy can cause lower obstruction and there this can lead to hydronephrosis of the kidney.

Question 9

What can cause post renal AKI

Answer 9

Physical obstructions at any levels:

Extra luminal - Mass, ovarian carcinoma pressing on ureters
Intra luminal - Stones
Prostate or urethra obstruction

Question 10

What is the pathophysiology of obstructive uropathy

Answer 10

Massive decrease in GFR due to loss of gradient, hydronephrosis. Usually is relieved with obstruction relief

Question 11

What can prolonged obstruction cause

Answer 11

Glomerular ischaemia
Tubular damage
Long term interstitial scarring

Question 12

What can cause direct tubular injury

Answer 12

Ischaemia - ATN
Endogenous toxins - Myoglobin and immunoglobulins in myeloma
Exogenous toxins - Aminoglycosides (Gentamicin), aciclovir, amphotericin

Question 13

What happens in rhabdomylosis

Answer 13

Myoglobin damage. A lot of bruising and dark (almost black) urine. Give patient a lot of fluids to wash out the myoglobin.

Question 14

How does systemic vasculitis present?

Answer 14

Widespread purpuric non blanching rash. AKI with glomerulunephritis and vasculitis

Question 15

What can cause abnormal protein deposition in renal tubules?

Answer 15

Amyloidosis, Lymphoma and myeloma related renal disease

Question 16

What 2 parameters are used to quantify severity of AKI

Answer 16

Serum creatinine and urine output

Question 17

Why does AKI progress to CKD?

Answer 17

First you stop the damage and/or bleeding. Next there is the inflammation cascade and scar tissue formation. Then the scar tissue needs to be remodelled to functional viable tissue. There is progress to CKD when there is an imbalance between scarring and remodelling.

Question 18

How is CKD staged?

Answer 18

Stages 1 to 5 based on GFR and albumin:creatinine ratio

Question 19

What causes CKD

Answer 19

Diabetes, hypertension, obstructive uropathy, atherosclerotic renal disease, chronic glomerulonephritis, polycystic kidney disease

Question 20

What hormones does the kidney produce?

Answer 20

EOP for RBCs, RAS, 1 alpha hydroxylase for vit d synthesis

Question 21

How does CKD cause a dysfunction. of the kidneys metabolic function?

Answer 21

It can cause metabolic acidosis and hyperkalaemia. Acidosis can cause muscle and protein degeneration and needs to be treated with oral sodium bicarbonate. Monitor patient levels to maintain above 20mmol/L

Hyperkalaemia can cause muscle depolarisation in cardiac and muscle function.

Question 22

What ecg changes can be seen in hyperkalaemia

Answer 22

Flattened p waves and tall peaked t waves. Prolonged qrs complex. Can lead to VT

Question 23

What medications can cause hyperkalaemia

Answer 23

ACEi, potassium sparing diuretics, spironolactone

Question 24

How is there anaemia in CKD

Answer 24

Kidneys stops producing EPO when GFR < 30ml/min. This results in normocytic normochromic anaemia. You can treat with EOP alpha or beta or darboprotein

Question 25

What anaemia do you see in iron deficiency

Answer 25

Microcytic, hypochromic

Question 26

What anaemia do you see in b12 folate deficiency

Answer 26

Macrocytic, reticulocytes

Question 27

How does CKD lead to hyperparathyroidism

Answer 27

Kidneys cannot excrete PO4, this will cause activation of FGF23 and Klotho which lowers vitamin D. Since there is no alpha hydroxylation of Vit D, PTH production will increase to get rid of PO4 and increase vit D production.

Question 28

How does CKD lead to hypocalcaemia

Answer 28

Increased phosphate will form complexes with free calcium, therefore reducing serum calcium levels. Lack of Vit D leads to less calcium too.

Question 29

What does CKD lead to eventually in terms of PTH

Answer 29

Tertiery hyperparathyroidism as the bones become resistant to the high levels of PTH.

Question 30

What are 3 types of bone diseases caused by CKD

Answer 30

Osteoitis fibrosa cystica, osteomalacia and adynamic bone disease

Question 31

What happens in osteoitis fibrosa cystica and what can you see

Answer 31

Increase osteoclastic reabsoprtion of calcified bone and formation of fibrous tissue.

Cystic lesions

Question 32

What is adynamic bone disease

Answer 32

Due to overtreatment and oversupression of PTH. Leads to reduced turnover and reduced osteoid.

Question 33

What happens in CKD and cardiovascular disease

Answer 33

Heavy calcification of arteries instead of cholestrol rich atheromas

Question 34

What are the 3 stages of uraemic cardiomyopathy

Answer 34

LV hypertrophy
LV dilation
LV dysfunction

Question 35

How do you treat excess phosphate?

Answer 35

Diet control and phosphate binders

Question 36

What are some vit D activators

Answer 36

1 alpha calcidol

Paricalcitol

Question 37

What are some direct PTH suppressors

Answer 37

Cinacalcet which works by increasing calcium sensing receptors